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    ALKALI INGESTION

    DEFINITION

    Intake through the mouth or nose and subsequent swallowing of a
    chemical which, in solution, has a pH > 7.0 and is of sufficient
    strength or quantity to result in injury to tissues.

    TOXIC CAUSES 

    Any solution with an alkaline pH has the potential to cause tissue
    injury when ingested.  The extent of injury depends not only on pH but
    also on the volume ingested, contact time, viscosity and
    concentration. Significant pathology is most commonly observed
    following ingestions of ammonia, potassium hydroxide, sodium hydroxide
    or sodium hypochlorite.

    CLINICAL FEATURES

    Symptoms and signs associated with significant alkali-induced tissue
    injury include pain in the mouth and throat, drooling, pain on
    swallowing, vomiting, abdominal pain and haematemesis.  If the larynx
    is involved, local oedema may produce respiratory distress, stridor
    and a hoarse voice.  

    Extensive tissue injury may be associated with fever, tachycardia,
    hypotension and tachypnoea.

    Inspection of the oropharynx may reveal areas of mucosal burn, which
    appear as white or grey patches with erythematous borders.  The
    absence of visible burns to the lips, mouth or throat does not
    necessarily imply an absence of significant burns to the oesophagus.

    Severe burns from alkali ingestion may lead to the life-threatening
    complications of oesophageal perforation and mediastinitis.  These are
    associated with chest pain, dyspnoea, fever, subcutaneous emphysema of
    the chest or neck, and a pleural rub.  A chest X-ray may show widening
    of the mediastinum, pleural effusions, pneumomediastinum and/or
    pneumothorax.  Septic shock, multi-organ failure and death may
    complicate perforation. 

    Tracheoesophageal fistulae may result from perforation of the anterior
    oesophageal wall.  The fistula may extend to involve the aorta and, in
    this case, is fatal.

    An asymptomatic patient is unlikely to have severe injury although
    asymptomatic children may occasionally have a significant injury.

    DIFFERENTIAL DIAGNOSIS

    Acid ingestion
    Allergic reaction with upper airways involvement
    Foreign body ingestion
    Other caustic ingestion 
    Thermal burn
    Upper airways infection

    RELEVANT INVESTIGATIONS

    Upper gastrointestinal endoscopy should be performed as soon as
    practicable and within 24 hours of ingestion.  This investigation is
    essential to assess the severity of mucosal damage and plan treatment. 
    Upper gastrointestinal endoscopy should also be considered for
    asymptomatic patients who have intentionally ingested a strong alkali
    and children, where the history may be unreliable.

    The following investigations may be useful to evaluate compliations
    and assist in management:

         Arterial blood gas analysis
         Coagulation profile
         Complete blood count
         Contrast oesophagography or thoracic CT (to detect oesophageal
         perforation).
         ECG
         Electrolytes
         Glucose
         Liver and renal function
         Radiological studies: Chest x-ray, upright abdominal film
         Type and cross-match

    TREATMENT

     Immediate (first) aid
    Do not induce vomiting.
    Do not attempt neutralisation.
    Do not give oral fluids
    Do not give oral activated charcoal
    Do rinse any visible material from the mouth with water or saline

     Hospital treatment
    Initial management is primarily supportive.  Particular attention
    should be directed towards securing the airway, fluid resuscitation
    and provision of opioid analgesia.  Do not give activated charcoal as
    it will interfere with endoscopic evaluation. 

    Ongoing supportive care includes maintenance of adequate analgesia,
    fluid, electrolyte and pH balance, nutritional support, and monitoring
    for the development of complications.

    Subsequent management and prognosis is largely dictated by findings at
    upper gastrointestinal tract endoscopy.  These may be graded as
    follows:

         Grade I        Simple inflammation.
         Grade II       Few ulcerations, focal necrosis limited to part of
                        the oesophagus.
         Grade III      Multiple ulcerations, extensive necrosis involving
                        all of the oesophagus, massive haemorrhage.

    Grade I and II lesions should heal completely with supportive care
    alone and can be adequately managed on a general medical ward. 
    Patients with Grade I lesions will usually tolerate oral fluids but
    those with Grade II lesions may require a period of total parenteral
    nutrition or a feeding jejunostomy.  Those with grade III endoscopic
    findings require intensive care management, total parenteral nutrition
    or a feeding jejunostomy until healing is documented, and are likely
    to develop oesophageal strictures.

    Urgent laparotomy (without associated thoracotomy) with surgical
    resection of necrotic tissue and surgical repair is indicated in the
    presence of symptoms or signs of gastrointestinal perforation or where
    full thickness necrosis is found at endoscopy. 

    There is no clinical evidence that corticosteroids prevent the
    development of strictures following alkali ingestion. 

    Prophylactic broad-spectrum antibiotics are not indicated unless there
    is   evidence of gastrointestinal tract perforation or full thickness
    necrosis.

    CLINICAL COURSE AND MONITORING 

    Careful monitoring of respiratory, cardiovascular, and renal systems
    and fluid, electrolyte and acid-base balance is required.  Cases of
    severe injury should be admitted to an Intensive Care Unit.  Close
    observation is required until an evaluation of the gastrointestinal
    tract can be made (preferably by endoscopy) unless the patient has
    become symptom free by that time.

    Patients should be followed for at least one year following recovery
    from Grade II or III alkali ingestion.  Assessment should be directed
    toward nutritional status and any problems with swallowing.

    LONG-TERM COMPLICATIONS

    Those patients with grade III or circumferential grade II burns are at
    risk of developing an oesophageal stricture.  For this reason, these
    patients require follow-up evaluations that include endoscopic
    examination and/or contrast radiography until complete healing or
    stricture formation is documented.  Eighty percent of strictures
    produce symptoms within two months.  Oesophageal stricture formation
    requires long-term dilation or surgical repair.

    Survivors of alkali ingestion are at an increased risk of developing
    carcinoma of the oesophagus.  The average interval between the
    original injury and diagnosis of carcinoma is greater than 40 years.

    AUTHOR(S)/REVIEWERS

    Author:        Robert Dowsett
                   Consultant Toxicologist
                   Departments of Clinical Pharmacology and Emergency
                   Medicine
                   Westmead Hospital
                   Westmead, NSW 2145
                   Australia

    Peer Review:   Geneva 8/98: D. Jacobsen, L. Murray, J. Pronczuk.
                   Birmingham 3/99: T. Meredith, L. Murray, A. Nantel, J.
                   Szajewski.